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Biomedical subjects

Paul B Rock

Publications and source records attributed to Paul B Rock.

13 recordsLinked to original sources

Local luminance amplitude modulates the interpretation of shape-from-shading in textured surfaces.

The pattern of illumination on an undulating surface can be used to infer its 3-D form (shape-from-shading). But the recovery of shape would be invalid if the luminance changes actually arose from changes in reflectance. So how does vision distinguish variation in illumination from variation in reflectance to avoid illusory depth? When a corrugated surface is painted with an albedo texture, the variation in local mean luminance (LM) due to shading is accompanied by a similar modulation in local luminance amplitude (AM). This is not so for reflectance variation, nor for roughly textured surfaces. We used depth mapping and paired comparison methods to show that modulations of local luminance amplitude play a role in the interpretation of shape-from-shading. The shape-from-shading percept was enhanced when LM and AM co-varied (in-phase) and was disrupted when they were out of phase or (to a lesser degree) when AM was absent. The perceptual differences between cue types (in-phase vs out-of-phase) were enhanced when the two cues were present at different orientations within a single image. Our results suggest that when LM and AM co-vary (in-phase) this indicates that the source of variation is illumination (caused by undulations of the surface), rather than surface reflectance. Hence, the congruence of LM and AM is a cue that supports a shape-from-shading interpretation.

Contrast Sensitivity↗

Tau as a potential control variable for visually guided braking.

D. N. Lee (1976) described a braking strategy based on optical expansion in which the driver brakes so that the target's time-to-contact declines around a constant slope in the range -0.5 < or = tau < 0. The present results from a series of braking simulations confirm and extend earlier reports (E. H. Yilmaz & W. H. Warren, 1995) that performance is broadly compatible with the tau hypothesis. However, performance was not enhanced in situations that favored the estimation of tau, and unlike in earlier reports, performance deteriorated in the absence of a ground plane that provided information about speed and target distance. This finding suggests that the tau hypothesis does not provide a complete account of braking control.

Adult↗

A test of the tau-dot hypothesis of braking control in the real world.

A controlled experiment used instrumented vehicles in a real-world driving task to compare D. N. Lee's (1976) tau-dot hypothesis of braking control with an alternative based on the direct estimation and control of ideal deceleration (T. Yates, M. Harris, & P. Rock, 2004). Drivers braked to stop as closely as possible to a visual target from different starting speeds and times-to-contact. The data provided little support for the tau-dot hypothesis, and analysis suggested that braking in the real world is better explained by a direct deceleration strategy.

Acceleration↗

Cytokine responses at high altitude: effects of exercise and antioxidants at 4300 m.

PURPOSE: This study tested the hypothesis that antioxidant supplementation would attenuate plasma cytokine (IL-6, tumor necrosis factor (TNF)-alpha), and C-reactive protein (CRP) concentrations at rest and in response to exercise at 4300-m elevation. METHODS: A total of 17 recreationally trained men were matched and assigned to an antioxidant (N = 9) or placebo (N = 8) group in a double-blinded fashion. At sea level (SL), energy expenditure was controlled and subjects were weight stable. Then, 3 wk before and throughout high altitude (HA), an antioxidant supplement (10,000 IU beta-carotene, 200 IU alpha-tocopherol acetate, 250 mg ascorbic acid, 50 microg selenium, 15 mg zinc) or placebo was given twice daily. At HA, energy expenditure increased approximately 750 kcal.d(-1) and energy intake decreased approximately 550 kcal.d, resulting in a caloric deficit of approximately 1200-1500 kcal.d(-1). At SL and HA day 1 (HA1) and day HA13, subjects exercised at 55% of VO2peak until they expended approximately 1500 kcal. Blood samples were taken at rest, end of exercise, and 2, 4, and 20 h after exercise. RESULTS: No differences were seen between groups in plasma IL-6, CRP, or TNF-alpha at rest or in response to exercise. For both groups, plasma IL-6 concentration was significantly higher at the end of exercise, 2, 4, and 20 h after exercise at HA1 compared with SL and HA13. Plasma CRP concentration was significantly elevated 20 h postexercise for both groups on HA1 compared to SL and HA13. TNF-alpha did not differ at rest or in response to exercise. CONCLUSION: Plasma IL-6 and CRP concentrations were elevated following exercise at high altitude on day 1, and antioxidant supplementation did not attenuate the rise in plasma IL-6 and CRP concentrations associated with hypoxia, exercise, and caloric deficit.

Adult↗

Endocrine responses to acute and chronic high-altitude exposure (4,300 meters): modulating effects of caloric restriction.

High-altitude anorexia leads to a hormonal response pattern modulated by both hypoxia and caloric restriction (CR). The purpose of this study was to compare altitude-induced neuroendocrine changes with or without energy imbalance and to explore how energy sufficiency alters the endocrine acclimatization process. Twenty-six normal-weight, young men were studied for 3 wk. One group [hypocaloric group (HYPO), n = 9] stayed at sea level and consumed 40% fewer calories than required to maintain body weight. Two other groups were deployed to 4,300 meters (Pikes Peak, CO), where one group (ADQ, n = 7) was adequately fed to maintain body weight and the other [deficient group (DEF), n = 10] had calories restricted as above. HYPO experienced a typical CR-induced reduction in many hormones such as insulin, testosterone, and leptin. At altitude, fasting glucose, insulin, and epinephrine exhibited a muted rise in DEF compared with ADQ. Free thyroxine, thyroid-stimulating hormone, and norepinephrine showed similar patterns between the two altitude groups. Morning cortisol initially rose higher in DEF than ADQ at 4,300 meters, but the difference disappeared by day 5. Testosterone increased in both altitude groups acutely but declined over time in DEF only. Adiponectin and leptin did not change significantly from sea level baseline values in either altitude group regardless of energy intake. These data suggest that hypoxia tends to increase blood hormone concentrations, but anorexia suppresses elements of the endocrine response. Such suppression results in the preservation of energy stores but may sacrifice the facilitation of oxygen delivery and the use of oxygen-efficient fuels.

Adaptation, Physiological↗

Three weeks of caloric restriction alters protein metabolism in normal-weight, young men.

The effects of prolonged caloric restriction (CR) on protein kinetics in lean subjects has not been investigated previously. The purpose of this study was to test the hypotheses that 21 days of CR in lean subjects would 1) result in significant losses of lean mass despite a suppression in leucine turnover and oxidation and 2) negatively impact exercise performance. Nine young, normal-weight men [23 +/- 5 y, 78.6 +/- 5.7 kg, peak oxygen consumption (Vo2 peak) 45.2 +/- 7.3 ml.kg(-1).min(-1), mean +/- SD] were underfed by 40% of the calories required to maintain body weight for 21 days and lost 3.8 +/- 0.3 kg body wt and 2.0 +/- 0.4 kg lean mass. Protein intake was kept at 1.2 g.kg(-1).day(-1). Leucine kinetics were measured using alpha-ketoisocaproic acid reciprocal pool model in the postabsorptive state during rest and 50 min of exercise (EX) at 50% of Vo2 peak). Body composition, basal metabolic rate (BMR), and exercise performance were measured throughout the intervention. At rest, leucine flux (approximately 131 micromol.kg(-1).h(-1)) and oxidation (R(ox); approximately 19 micromol.kg(-1).h(-1)) did not differ pre- and post-CR. During EX, leucine flux (129 +/- 6 vs. 121 +/- 6) and R(ox) (54 +/- 6 vs. 46 +/- 8) were lower after CR than they were pre-CR. Nitrogen balance was negative throughout the intervention ( approximately 3.0 g N/day), and BMR declined from 1,898 +/- 262 to 1,670 +/- 203 kcal/day. Aerobic performance (Vo2 peak, endurance cycling) was not impacted by CR, but arm flexion endurance decreased by 20%. In conclusion, 3 wk of caloric restriction reduced leucine flux and R(ox) during exercise in normal-weight young men. However, despite negative nitrogen balance and loss of lean mass, whole body exercise performance was well maintained in response to CR.

Adolescent↗

Saccadic velocity and pupillary reflexes during acclimatization to altitude (4300 m).

INTRODUCTION: Oculometrics have been shown to be responsive to acute hypoxemia. We investigated whether oculometrics could be used as an objective index of a hypoxic effect on the central nervous system (CNS) during altitude acclimatization. We hypothesized that oculomotor reflexes [pupil diameter (PD), constriction amplitude (CA), constriction latency (CL), and saccadic velocity (SV)] changed in concert with a select number of accepted acclimatization variables and that these changes correlated with the severity of acute mountain sickness (AMS). METHODS: After sea-level, baseline (SLB) measurements were obtained, 18 men (19-33 yr) were transported to Pikes Peak, CO (4300 m), where they remained for 14 d. Periodic measurements (days 1-4, 6, 7, 9, 10, and 12) were made of PD, CA, CL, and SV in addition to heart rate (HR), pulse oximetry (SpO2), end-tidal PO2 and PCO2, 24-h urinary catecholamine concentrations, and AMS severity (environmental symptoms questionnaire, ESQ). RESULTS: PD and CL decreased from SLB on days 1-4 and subsequently returned toward SLB; these changes paralleled changes in ventilatory and circulatory variables. CA decreased on days 1 and 2 and remained decreased for 12 d. SV increased over days 1-6 then returned toward SLB with continued exposure, similar to changes in urinary catecholamines. With acclimatization, CL correlated with HR and SpO2; SV correlated with PCO2, HR, and SpO2. AMS severity peaked during days 2-4, returned toward SLB over the next 10 d, and correlated only with CL (p = 0.045). CONCLUSIONS: Oculometrics can be used as an indicator of CNS hypoxia and altitude acclimatization, although there was no strong correlation with AMS severity.

Acclimatization↗

Ventilation after supplemental oxygen administration at high altitude.

OBJECTIVE: The present study assessed the effects of acute hyperoxia on resting-minute ventilation (VE) during altitude acclimatization to 4300 m. METHODS: Resting-minute ventilation, end-tidal partial pressure carbon dioxide (PETCO2) and oxygen (P(ET)O2), and arterial oxygen saturation (SpO2) were measured during chronic poikilocapnic hypobaric hypoxia, supplemental oxygen breathing, and the subsequent return to hypobaric poikilocapnic hypoxia at altitude. Fifteen adult male lowlanders were studied at sea level and on the 3rd and 12th days at 4300 m. At sea level, subjects first breathed room air that was followed by 25-minute steady-state poikilocapnic hypoxia (FIO2 = 0.125). Ventilatory responses to acute poikilocapnic hypoxia (APH) were collected over the first 1-10 minutes, and responses to chronic poikilocapnic hypoxia (CPH) were collected over the last 3 minutes of the hypoxia exposure. At altitude, CPH was provided by ambient-air breathing (PIO2 = 86 mm Hg) that was interrupted by 10 minutes of oxygen breathing (FIO2 = 1.0, PIO2 = 460 mm Hg) and then a subsequent return to ambient air to measure APH ventilatory responses. RESULTS: Between day 1 and day 12, during CPH, VE and SpO2 increased (P < .05) by 46% and 6%, respectively, whereas P(ET)CO2 decreased. On day 3 and day 12, breathing oxygen did not lower VE compared with CPH. However, the VE during APH immediately after oxygen breathing at high altitude was always greater (P < .05) than during CPH and did not change with duration of residence at altitude. CONCLUSIONS: These results show that short-duration oxygen breathing increases the subsequent ventilatory response to poikilocapnic hypoxia in altitude-acclimatized lowlanders, resulting in a transient elevation of SpO2.

Acclimatization↗

Antioxidant supplementation does not attenuate oxidative stress at high altitude.

INTRODUCTION: Hypobaric hypoxia and heightened metabolic rate increase free radical production. PURPOSE: We tested the hypothesis that antioxidant supplementation would reduce oxidative stress associated with increased energy expenditure (negative energy balance) at high altitude (HA 4300 m). METHODS: For 12 d at sea level (SL), 18 active men were fed a weight-stabilizing diet. Testing included fasting blood and 24-h urine samples to assess antioxidant status [plasma alpha-tocopherol, beta-carotene, lipid hydroperoxides (LPO), and urinary 8-hydroxydeoxyguanosine (8-OHdG)] and a prolonged submaximal (55% Vo2peak) oxidative stress index test (OSI) to evaluate exercise-induced oxidative stress (plasma LPO, whole blood reduced and oxidized glutathione, glutathione peroxidase, and urinary 8-OHdG). Subjects were then matched and randomly assigned to either a placebo or antioxidant supplement group for a double-blinded trial. Supplementation (20,000 IU of beta-carotene, 400 IU alpha-tocopherol acetate, 500 mg ascorbic acid, 100 microg selenium, and 30 mg zinc, or placebo) was begun 3 wk prior to and throughout a 14-d HA intervention. At HA, subjects' daily energy intake and expenditure were adjusted to achieve a caloric deficit of approximately 1400 kcal. Fasting blood and 24-h urine samples were collected throughout HA and the OSI test was repeated on HA day 1 and day 13. RESULTS: Resting LPO concentrations increased and urinary 8-OHdG concentrations decreased over HA with no effect of supplementation. Prolonged submaximal exercise was not associated with increased concentrations of oxidative stress markers at SL or HA. CONCLUSIONS: Antioxidant supplementation did not significantly affect markers of oxidative stress associated with increased energy expenditure at HA.

Adult↗

Residence at moderate altitude improves ventilatory response to high altitude.

BACKGROUND: This study compared the distribution of arterial oxygen saturation (SaO2) and susceptibility to Acute Mountain Sickness (AMS) in moderate altitude residents (MAR) and low altitude residents (LAR) following rapid ascent to 4056 m. METHODS: Resting PETCO2 and SaO2 were measured in 38 subjects residing for > 3 mo near Colorado Springs, CO (MAR group), at 1940 m (USAF Academy), and after approximately 1 h at 4056 m on the summit of Pikes Peak, CO, following ascent by car. SaO2 was also measured at 610-m elevation intervals during the ascent. Of the LAR (50 m) group, 39 subjects were exposed to a similar ascent profile in a hypobaric chamber. RESULTS: At 1940 m the MAR SaO2 and PETCO2 were 94 +/- 1% (X +/- SD) and 33.6 +/- 2.8 mmHg, respectively. At 3048 m and higher, MAR SaO2 decreased, reaching 86 +/- 2% (p < 0.001) at 4056 m, and PETCO2 (32.1 +/- 4.5 mmHg) decreased (p < 0.05). At 50 m the LAR SaO2 and PETCO2 were 98 +/- 1% and 38.7 +/- 2.7 mmHg, respectively. At 1940 m and higher, LAR SaO2 decreased (p < 0.001), reaching 82 +/- 5% at 4056 m, and PETCO2 (36.4 +/- 3.5 mmHg) decreased (p < 0.05). Above 2438 m, the MAR SaO2 was higher (p < 0.001) than the LAR. Only one MAR subject, but nine LAR subjects reported AMS symptoms. CONCLUSIONS: Ventilatory acclimatization developed during moderate altitude residence substantially enhances arterial oxygenation during rapid ascents to higher altitudes. Compared with prior studies, the level of ventilatory acclimatization achieved at moderate altitude is similar to residing at 4056 m for approximately 5-9 d.

Adaptation, Physiological↗

Influence of alpha-adrenergic blockade on the catecholamine response to exercise at 4,300 meters.

This investigation examined the influence of alpha-adrenergic blockade on plasma and urinary catecholamine responses to both exercise and high-altitude exposure. Sixteen nonsmoking, eumenorrheic women (age 23.2 +/- 1.4 years, 68.7 +/- 1.0 kg) were studied at sea level and during 12 days of high-altitude exposure (4,300 m). Subjects received either alpha-blockade (prazosin 3 mg/d) or a placebo in a double-blinded, randomized fashion. Resting plasma and 24-hour urine samples were collected periodically throughout the duration of the study. Further, subjects participated in submaximal exercise tests (50 minutes at 50% sea level maximum oxygen consumption [Vo2max]) at Sea level and on days 1 and 12 at altitude. Urinary norepinephrine (NE) excretion rates increased significantly over time at altitude, with blocked subjects having greater values compared to controls. Plasma NE levels increased significantly with chronic altitude exposure compared to sea level and acute hypoxia both at rest and during exercise. NE levels at rest were greater for blocked compared to control subjects during all conditions. Urinary and plasma epinephrine (EPI) levels increased dramatically, with acute altitude exposure returning to sea level values by day 12 of altitude exposure. EPI levels were greater for blocked compared to placebo both at rest and during exercise for all conditions studied. Changes in alpha-adrenergic activity over time at altitude were associated with select metabolic and physiologic adjustments. The presence of alpha-blockade significantly affected these responses during chronic altitude exposure. It was concluded that: (1) alpha-adrenergic blockade elicited a potentiated sympathoadrenal response to the stress of both exercise as well as high-altitude exposure, and (2) the sympathetics, via alpha-adrenergic stimulation, contribute to a number of key adaptations associated with acclimatization to high altitude.

Acclimatization↗

Substrate oxidation is altered in women during exercise upon acute altitude exposure.

PURPOSE: The purpose of this study was to determine whether substrate oxidation during submaximal exercise in women is affected by an acute exposure to 4300-m altitude and menstrual cycle phase. METHODS: Eight female lowlanders (mean +/- SD; 33 +/- 3 yr, 58 +/- 6 kg, 163 +/- 8 cm) completed a peak oxygen uptake (VO2peak) and submaximal exercise to exhaustion (EXH) test at 70% of their altitude-specific VO2peak at sea level (SL) and during an acute altitude (AA) exposure to 4300 m in a hypobaric chamber (446 mm Hg) in their early-follicular and midluteal menstrual cycle phase. The respiratory exchange ratio (RER) was calculated from oxygen uptake and carbon dioxide output measurements made during the EXH tests, and used to estimate the percent contribution of fat and carbohydrate to energy metabolism. Blood samples were taken at rest and every 15 min during the EXH tests. Blood samples were evaluated for glucose, lactate, glycerol, free fatty acids, insulin, growth hormone, cortisol, glucagon, epinephrine, norepinephrine, estradiol, and progesterone concentrations. RESULTS: Despite increased (P < 0.05) estradiol and progesterone levels in the midluteal phase, substrate oxidation, energy substrates, and metabolic hormones were not affected by cycle phase at SL or AA. However, free fatty acids and cortisol were increased (P < 0.05) whereas RER was decreased (P < 0.05) during exercise upon AA exposure compared with SL in both cycle phases. CONCLUSIONS: These data suggest that substrate oxidation is altered in women during exercise at AA compared with SL but is not affected by cycle phase. Whether increased fat or protein oxidation accounts for the lower RER values during the AA exposure cannot be determined from this study but warrants further investigation.

Adult↗

Speech motor control and acute mountain sickness.

BACKGROUND: An objective method that accurately quantifies the severity of Acute Mountain Sickness (AMS) symptoms is needed to enable more reliable evaluation of altitude acclimatization and testing of potentially beneficial interventions. HYPOTHESIS: Changes in human articulation, as quantified by timed variations in acoustic waveforms of specific spoken words (voice onset time; VOT), are correlated with the severity of AMS. METHODS: Fifteen volunteers were exposed to a simulated altitude of 4300 m (446 mm Hg) in a hypobaric chamber for 48 h. Speech motor control was determined from digitally recorded and analyzed timing patterns of 30 different monosyllabic words characterized as voiced and unvoiced, and as labial, alveolar, or velar. The Environmental Symptoms Questionnaire (ESQ) was used to assess AMS. RESULTS: Significant AMS symptoms occurred after 4 h, peaked at 16 h, and returned toward baseline after 48 h. Labial VOTs were shorter after 4 and 39 h of exposure; velar VOTs were altered only after 4 h; and there were no changes in alveolar VOTs. The duration of vowel sounds was increased after 4 h of exposure and returned to normal thereafter. Only 1 of 15 subjects did not increase vowel time after 4 h of exposure. The 39-h labial (p = 0.009) and velar (p = 0.037) voiced-unvoiced timed separations consonants and the symptoms of AMS were significantly correlated. CONCLUSIONS: Two objective measures of speech production were affected by exposure to 4300 m altitude and correlated with AMS severity. Alterations in speech production may represent an objective measure of AMS and central vulnerability to hypoxia.

Acclimatization↗